Crystallization and crystal structure of the β phase of oleic acid (cis-9-octadecenoic acid) have been investigated with morphological observation, X-ray diffraction, and DSC (differential scanning calorimeter). The morphology of growing crystals of the β phase depends significantly on supercooling. It was found that the β phase could be classified into at least two solid modifications, β1 (mp 16.3 °C) and β2 (mp 16.0 °C). The crystal structure analysis of the β1 phase has been performed. The unit cell belongs to a triclinic system of P1̄, and the asymmetric unit contains two crystallographically independent molecules, A and B. The molecular layer is a unique interdigitated structure, where the methyl group of molecule A and the carboxyl group of molecules B (or vice versa) are located on the same plane. For the conformation around the cis-CC bond, both molecules approximate to trans−cis−trans conformation, the first case for a cis-monounsaturated fatty acid. The methyl and carboxyl side chains together form a T∥ subcell. On the basis of its crystal structure, it was speculated that the β1 phase has a unique surface structure at the (001) face. The factors for the characteristic properties of the β phase were also discussed.

Taurine (2-aminoethanesulfonic acid) is a potent antioxidant and inhibits cell apoptosis in ischemic reperfusion injury. In this study we evaluated whether addition of taurine to St. Thomas' cardioplegic solution enhances its myocardial protective effects in prolonged hypothermic heart preservation in rats. Hearts isolated from male Sprague-Dawley rats were mounted on a Langendorff apparatus to estimate baseline cardiac function, then arrested and stored in St. Thomas' cardioplegic solution, with taurine (10 mM; taurine group, n = 8) or without taurine (control group, n = 8), for 6 h at 4 degrees C. After storage, the hearts were reperfused and heart rate (HR), coronary flow (CF), left ventricular developed pressure (LVP), and positive maximum left ventricular developing pressure (max LV dp/dt) were measured. The LV tissue was examined immunohistochemically for determining DNA oxidative stress and cell apoptosis. Compared with control groups, recovery of LVP (P < 0.001), max LV dp/dt (P < 0.001), and coronary flow (P < 0.001) were significantly enhanced, whereas glutamic oxaloacetic transaminase (P < 0.01), lactate dehydrogenase (P < 0.05), creatine phosphate kinase (P < 0.01), 8-hydroxy-2'-deoxyguanosine index (P < 0.01), caspase-3 mRNA expression (P < 0.05), and percentage of TUNEL-positive cardiomyocytes (P < 0.05) were reduced in the taurine group. Addition of taurine to St. Thomas' cardioplegic solution improved cardiac function recovery for prolonged hypothermic rat heart preservation by suppressing DNA oxidative stress and cell apoptosis.

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Nonviral transduction of miR-145 into the bypass graft could be a novel option for preventing intimal hyperplasia in vein graft disease.

Preoperative oral administration of EGCG ameliorates AKI in a CPB model of diabetic rats through antioxidative properties. This simple method could be applied in a clinical setting as a prophylactic renal protection against AKI after CPB, especially for high-risk patients with diabetes mellitus.

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Background: Cardiopulmonary bypass (CPB) may induce systemic inflammatory responses causing acute lung injury. Recombinant human soluble thrombomodulin (rTM) is reported to attenuate the secretion of inflammatory cytokines and the high-mobility group box 1 (HMGB1) protein, which is critical in controlling systemic inflammation and apoptosis. We investigated the protective effects of rTM on CPB-induced lung injury in a rat model. Methods: Eighteen male Sprague-Dawley rats were divided into 3 groups: sham, control (CPB alone), and rTM (CPB þ rTM). CPB was conducted in the control group and the rTM group. A bolus of rTM (3 mg/kg) was administered to the rTM group rats before CPB establishment. Results: The ratio of partial pressure of arterial oxygen to the fraction of inspired oxygen only dropped markedly from before CPB in the control group (P<.001). Serum tumor necrosis factor a, interleukin (IL) 6, and HMGB1 levels were significantly higher in the control group after CPB. Pathologic study revealed significantly more severe congestion, alveolar hemorrhage, neutrophil accumulation, and edema, and the number of lung cells expressing HMGB1 increased in the control group. The mRNA expression levels of tumor necrosis factor a, IL-6, IL-1b, and HMGB1 in the control group were significantly higher than those in other groups. According to Western blot analysis, nuclear factor-kB p65 in lung tissue was significantly downregulated in the rTM group. The number of apoptotic cells and the protein of cleaved Caspase-3 were reduced in the rTM group. Conclusions: These results suggest that rTM prevents acute lung injury through attenuating inflammation and apoptosis during and after CPB in a rat model. (

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